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J Am Coll Cardiol, 2008; 52:29, doi:10.1016/S0735-1097(08)03881-3
© 2008 by the American College of Cardiology Foundation
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INSIDE THIS ISSUE OF JACC

Inside This Issue of JACC


    State-of-the-Art Paper
 Top
 State-of-the-Art Paper
 Clinical Trials
 Clinical Trials
 Cardiovascular Risk
 Cardiovascular Risk
 Biomarkers in Heart Failure
 Arrhythmogenic Cardiomyopathy
 
Understanding the Techniques Used in Cost Effectiveness Studies.   This review by Cohen and Reynolds provides an introduction to cost-effectiveness analyses in order to help readers understand and interpret these studies. Cost minimization studies try to establish the least costly intervention among clinically equivalent strategies. Cost-effectiveness studies calculate incremental monetary costs, compared with clinical benefits, which are expressed in nonmonetary terms, such as life years gained or adverse events avoided. These types of studies are hampered by a lack of consensus on what dollar threshold per outcome should be considered effective and other factors, such as cost shifting, otherwise known as payer perspective, and extrapolated time horizons, which may extend beyond the length of the underlying clinical trial data. See page 2119.


    Clinical Trials
 Top
 State-of-the-Art Paper
 Clinical Trials
 Clinical Trials
 Cardiovascular Risk
 Cardiovascular Risk
 Biomarkers in Heart Failure
 Arrhythmogenic Cardiomyopathy
 
Bosentan for Inoperable CTEPH.  
Figure 1
There is currently no approved medical therapy for inoperable or persistent/recurrent chronic thromboembolic pulmonary hypertension (CTEPH). Jaïs and colleagues hypothesized that bosentan, which is effective for idiopathic pulmonary artery hypertension (PAH), as well as PAH associated with other conditions, would be effective. Over 150 patients were randomized to bosentan or placebo for 16 weeks. Bosentan significantly reduced pulmonary vascular resistance (PVR) and improved the cardiac index, but failed to improve 6-minute walk distance. Further trials are needed to ascertain whether the improved PVR will result in long term clinical benefits, but the treatment was well-tolerated and appears promising. See page 2127. See figure.


    Clinical Trials
 Top
 State-of-the-Art Paper
 Clinical Trials
 Clinical Trials
 Cardiovascular Risk
 Cardiovascular Risk
 Biomarkers in Heart Failure
 Arrhythmogenic Cardiomyopathy
 
Multivendor Trial of CTCA Shows Good Diagnostic Accuracy.  
Figure 2
Meijboom and colleagues performed computed tomographic coronary angiography (CTCA) on patients referred for standard catheterization using machines from 3 different vendors and at 3 different medical centers. No patients who met the study criteria were excluded for poor image quality; likewise, no coronary artery segments were excluded. In a patient-based analysis, the sensitivity for significant CAD was 99%, positive predictive value was 86%, and negative predictive value was 97%. In a segment-based analysis, the positive predictive value was lower at 47% because of "over-reading" of lesions <50% diameter stenosis, many of which were calcified. 64-slice CTCA can reliably rule out significant coronary artery disease, but may overestimate the severity of some obstructions. See pages 2135 and 2145. See figure.


    Cardiovascular Risk
 Top
 State-of-the-Art Paper
 Clinical Trials
 Clinical Trials
 Cardiovascular Risk
 Cardiovascular Risk
 Biomarkers in Heart Failure
 Arrhythmogenic Cardiomyopathy
 
LV Mass Strongly Linked to HF.  
Figure 3
This study evaluated the relationship of left ventricular (LV) mass and geometry measured with cardiac magnetic resonance imaging (MRI) to incident cardiovascular events. An increased LV mass to volume ratio was associated with stroke and coronary heart disease, which included angina, heart failure (HF), and myocardial infarction. Subjects with an LV mass >95th percentile were 8 times more likely to be diagnosed with HF compared with those with an LV mass <50th percentile. This study confirms the link between increased LV mass and cardiovascular outcomes, and provides guidance on the most appropriate MRI-based measurements. See page 2148. See figure.


    Cardiovascular Risk
 Top
 State-of-the-Art Paper
 Clinical Trials
 Clinical Trials
 Cardiovascular Risk
 Cardiovascular Risk
 Biomarkers in Heart Failure
 Arrhythmogenic Cardiomyopathy
 
Link Between Stress and CVD Is Behavior.   Although the association between psychological distress and cardiovascular risk is known, the mechanisms are not. Hamer and colleagues studied this link in over 6,000 people. Psychological stress was measured with the 12-item version of the General Health Questionnaire. Subjects were also questioned about behavioral issues (smoking, alcohol intake, physical activity) and were assessed for other cardiac risk factors. Over 7 years of follow-up, the risk of cardiovascular disease (CVD) increased with increased psychological distress. Behavioral factors explained the largest proportion of variance (~65%). These data suggest that the behavioral factors of smoking and physical inactivity are a significant link between psychological distress and increased cardiac risk. See pages 2156 and 2163.


    Biomarkers in Heart Failure
 Top
 State-of-the-Art Paper
 Clinical Trials
 Clinical Trials
 Cardiovascular Risk
 Cardiovascular Risk
 Biomarkers in Heart Failure
 Arrhythmogenic Cardiomyopathy
 
ST2 Correlates With LVEDP; Produced by Endothelium Not Myocardium.  
Figure 4
Serum ST2 is a recently identified biomarker for patients with myocardial infarction and/or congestive heart failure. Bartunek and colleagues measured serum ST2 levels in patients with pressure overload hypertrophy secondary to aortic stenosis (AS) and congestive cardiomyopathy (CCM). The ST2 was elevated in patients with AS and CCM and correlated with B-type natriuretic peptide, C-reactive protein, and left ventricular end-diastolic pressure (LVEDP). There was no difference in ST2 levels between the coronary sinus and the aorta, suggesting that ST2 is not made in the myocardium. Further studies confirmed that ST2 is produced in endothelial cells, not myocardial cells. Serum ST2 correlates with diastolic load, but the source of serum ST2 is extra-myocardial. See page 2166. See figure.


    Arrhythmogenic Cardiomyopathy
 Top
 State-of-the-Art Paper
 Clinical Trials
 Clinical Trials
 Cardiovascular Risk
 Cardiovascular Risk
 Biomarkers in Heart Failure
 Arrhythmogenic Cardiomyopathy
 
Characteristics of LDAC.   Sen-Chowdhry and colleagues describe a cohort of patients whom they hypothesized had a left dominant subtype of arrhythmogenic right ventricular cardiomyopathy (ARVC) that they term left dominant arrhythmogenic cardiomyopathy (LDAC). Subjects were recruited who had unexplained (infero)lateral T-wave inversion, arrhythmia of left ventricular (LV) origin, and/or a relative with LDAC. Presenting symptoms were arrhythmia or chest pain, but not heart failure. Desmosomal mutations, which are thought to cause ARVC, were found in one-third of the families and one-half of the subjects. Cardiac magnetic resonance imaging showed LV late-enhancement in a subepicardial/midwall distribution. LDAC appears to be a variant of ARVC; the authors suggest that the terminology be changed to "arrythmogenic cardiomyopathy with subtypes of right, left, and biventricular." See pages 2175 and 2188.


Related Articles

Interpreting the Results of Cost-Effectiveness Studies
David J. Cohen and Matthew R. Reynolds
J. Am. Coll. Cardiol. 2008 52: 2119-2126. [Abstract] [Full Text] [PDF]

Bosentan for Treatment of Inoperable Chronic Thromboembolic Pulmonary Hypertension: BENEFiT (Bosentan Effects in iNopErable Forms of chronIc Thromboembolic pulmonary hypertension), a Randomized, Placebo-Controlled Trial
Xavier Jaïs, Andrea M. D'Armini, Pavel Jansa, Adam Torbicki, Marion Delcroix, Hossein A. Ghofrani, Marius M. Hoeper, Irene M. Lang, Eckhard Mayer, Joanna Pepke-Zaba, Loïc Perchenet, Adele Morganti, Gérald Simonneau, Lewis J. Rubin for the BENEFiT Study Group
J. Am. Coll. Cardiol. 2008 52: 2127-2134. [Abstract] [Full Text] [PDF]

Diagnostic Accuracy of 64-Slice Computed Tomography Coronary Angiography: A Prospective, Multicenter, Multivendor Study
W. Bob Meijboom, Matthijs F.L. Meijs, Joanne D. Schuijf, Maarten J. Cramer, Nico R. Mollet, Carlos A.G. van Mieghem, Koen Nieman, Jacob M. van Werkhoven, Gabija Pundziute, Annick C. Weustink, Alexander M. de Vos, Francesca Pugliese, Benno Rensing, J. Wouter Jukema, Jeroen J. Bax, Mathias Prokop, Pieter A. Doevendans, Myriam G.M. Hunink, Gabriel P. Krestin, and Pim J. de Feyter
J. Am. Coll. Cardiol. 2008 52: 2135-2144. [Abstract] [Full Text] [PDF]

Limitations of Computed Tomography Coronary Angiography
Steven E. Nissen
J. Am. Coll. Cardiol. 2008 52: 2145-2147. [Full Text] [PDF]

The Relationship of Left Ventricular Mass and Geometry to Incident Cardiovascular Events: The MESA (Multi-Ethnic Study of Atherosclerosis) Study
David A. Bluemke, Richard A. Kronmal, João A.C. Lima, Kiang Liu, Jean Olson, Gregory L. Burke, and Aaron R. Folsom
J. Am. Coll. Cardiol. 2008 52: 2148-2155. [Abstract] [Full Text] [PDF]

Psychological Distress as a Risk Factor for Cardiovascular Events: Pathophysiological and Behavioral Mechanisms
Mark Hamer, Gerard J. Molloy, and Emmanuel Stamatakis
J. Am. Coll. Cardiol. 2008 52: 2156-2162. [Abstract] [Full Text] [PDF]

Psychological Distress and Cardiovascular Risk: What Are the Links?
Roland von Känel
J. Am. Coll. Cardiol. 2008 52: 2163-2165. [Full Text] [PDF]

Nonmyocardial Production of ST2 Protein in Human Hypertrophy and Failure Is Related to Diastolic Load
Jozef Bartunek, Leen Delrue, Frederik Van Durme, Olivier Muller, Filip Casselman, Bart De Wiest, Romaric Croes, Sofie Verstreken, Marc Goethals, Herbert de Raedt, Jaydeep Sarma, Lija Joseph, Marc Vanderheyden, and Ellen O. Weinberg
J. Am. Coll. Cardiol. 2008 52: 2166-2174. [Abstract] [Full Text] [PDF]

Left-Dominant Arrhythmogenic Cardiomyopathy: An Under-Recognized Clinical Entity
Srijita Sen-Chowdhry, Petros Syrris, Sanjay K. Prasad, Siân E. Hughes, Robert Merrifield, Deirdre Ward, Dudley J. Pennell, and William J. McKenna
J. Am. Coll. Cardiol. 2008 52: 2175-2187. [Abstract] [Full Text] [PDF]

Expanding the Spectrum of Arrhythmogenic Cardiomyopathy
Jeffrey E. Saffitz
J. Am. Coll. Cardiol. 2008 52: 2188-2189. [Full Text] [PDF]




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